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Aspartate Aminotransferase (AST)

Aspartate aminotransferase (AST) is an enzyme involved in the transfer of an amino group from aspartate to alpha ketoglutarate to produce oxaloacetic acid and glutamate.  AST is present in most organs. The highest concentrations, listed in descending order, are found in liver, heart, skeletal muscle, kidney, brain, pancreas, lung, leukocytes, and erythrocytes.  Because of its wide tissue distribution, elevated AST levels have low specificity for any single disease.  AST activities in liver are 7000 times higher than serum activities. Historically, AST has been used clinically to diagnose hepatitis, myocardial infarction, and skeletal muscle disease.  AST increase in the absence of ALT increase indicates cardiac or skeletal muscle disease.  ALT is a better indicator of liver disease, because of its more limited tissue distribution. 

AST tends to run slightly higher in males than females due to differences in body mass and varies with age.  AST is slightly higher than ALT until the age of 15 to 20 years. Thereafter, AST activity tends to be lower than ALT.  At age 60, AST and ALT activities become roughly equal.  AST levels are about 15% higher in African American than Caucasian men. Obese men may have mildly elevated AST levels. AST levels can fluctuate between 5 and 10% from one day to the next in the same individual.  Moderate exercise increases AST levels for as long as 24 hours, usually less than 3 times the upper limit of normal. The half-life of AST in the circulation is 17 +/- 5 hours

The ratio of AST to ALT in plasma may help in the diagnosis of some liver diseases. Most liver diseases are associated with greater elevation of ALT than AST because of differences in the circulating half-life of each enzyme and the cellular distribution.  ALT has a longer circulating half-life (47+/- 10 hours) than AST (17+/-5 hours). AST is distributed both in the cytoplasm and mitochondria of hepatocytes, while ALT is distributed mainly in the cytoplasm. Normal serum levels of AST are derived from the cytoplasmic fraction.  Mild cell injury results in release of cytoplasmic enzyme, while severe injury releases both cytoplasmic and mitochondrial AST.

Exceptions to this rule are seen in alcoholic hepatitis, Wilson disease and Reye syndrome. In alcoholic hepatitis, damage is primarily to the mitochondria and more AST is released than ALT.  In alcoholic hepatitis, the AST:ALT ratio is  2.0 or greater and the AST increase is seldom more than 300 U/L.  In contrast, viral hepatitis primarily damages the cell membrane, releasing more ALT than AST. The AST:ALT ratio is less than 1. The AST: ALT ratio is less useful in distinguishing alcoholic from other causes of hepatocellular injury in patients with cirrhosis, because the ratio is usually >1. 



Peak ALT x ULN


Peak Bilirubin

Protime Prolongation

Viral hepatitis

10 – 40




Alcoholic hepatitis

2 - 8



1 – 3

Toxic injury


>1 early


>5 transient

Ischemic injury


>1 early


>5 transient

The chronology and extent of AST elevation provides some insight into the etiology of the underlying liver disease.The highest serum levels occur in viral and toxic hepatitis and ischemic necrosis.

Liver Disease

AST Pattern


Early increase to peak of <5 times ULN and return to normal within 72 hours


Increase up to 10 times ULN

Viral hepatitis

Steady increase to peak level in low thousands at 7 - 14 days

Alcoholic hepatitis

Increase to <300

Ischemic injury

Abrupt increase within 24 hours to peak >10,000

Acetaminophen toxicity

Increase over 48 hours to peak >10,000

Nonalchololic steatosis can increase both AST and ALT. This condition occurs most commonly in middle aged women with obesity and/or diabetes., but is also associated with jejunoileal bypass surgery, total parenteral nutrition, and drugs such as amiodarone

Both hypo and hyperthyroidism can increase AST and ALT, usually less than three times the upper limit of normal.  Other causes of elevated ALT include hemochromatosis, Wilson disease, autoimmune hepatitis, primary biliary cirrhosis, sclerosing cholangitis and alpha-1 antitrypsin deficiency.

In a patient with increased transaminases, decreasing levels usually indicates clinical improvement.  However, a rapid decrease in a patient with acute hepatitis may indicate impending hepatic failure.  In this situation, the prothrombin time can be followed as a sensitive index of liver synthetic function. 

A rare cause of increased AST is the complexing of AST with an immunoglobulin, producing a macroenzyme that is not cleared from the circulation.  Macro-AST does not indicate underlying liver disease. 

Many medications can increase AST levels. The most common drugs are: acetaminophen, nonsteroidal anti-inflammatory drugs, angiotensin converting enzyme (ACE) inhibitors, nicotinic acid, isoniazid, sulfonamides, erythromycin, griseofulvin, and fluconazole.

Both AST and ALT require vitamin B6 (pyridoxal-5'-phosphate, P5P) as a catalytic cofactor. Pyridoxal-5’-phosphate deficiency is common in alcoholic liver disease, malnutrition and renal failure. Patients with these disorders may have results below the reference range.  In an attempt to standardize aminotransferase assays, the International Federation of Clinical Chemistry (IFCC) recommended that laboratories add excess P5P to their enzyme reagents so that these assay accurately measure enzyme activity independently of vitamin B6 status. Unfortunately, less than 50% of ALT assays incorporate exogenous 5P5.

Reference range is 15 – 41 IU/L

Specimen requirement is one red top or green top tube of blood.

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